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cytosolic ca
The results obtained indicate that an early rise in cytosolic Ca2+ as well as a quick establishment of ionic homeostasis may be essential for the induction of adaptive changes at the cellular as well as organismal level.
      
Apparently, La3+, a Ca2+ channel blocker, inhibits the changes in the cytosolic Ca2+ concentration in guard cells, thus affecting stomatal movements.
      
A possible role of cytosolic Ca2+ rise in the mechanism of photosynthesis suppression after electric excitation of the plasma membrane is discussed.
      
Moreover, an increase of cytosolic Ca2+ was revealed in the cells exposed to FA, which could be explained by the activation of plasma membrane calcium channels.
      
The Ca2+-dependent SV channel can be activated by cytosolic Ca2+.
      
The second section deals with the predominant role of cytosolic Ca2+ as a second messenger controlling cell function.
      
In re-energized cardiomyocytes, a persistent elevation of the cytosolic Ca2+ concentration provokes maximal force development and consecutive mechanical cell injury ("oxygen paradox").
      
This injury can be prevented when the contractile machinery is inhibited during the initial phase of reoxygenation as long as necessary for the re-establishment of a normal cytosolic Ca2+ control.
      
In the control group reoxygenation provoked oscillations of cytosolic Ca2+ (60.9±9.6 min-1 at 5 min of reoxygenation) accompanied by development of hypercontracture (to 77.2±3.8% of end-ischemic cell length).
      
Cytosolic Ca2+ overload plays a major role in the development of irreversible injury during myocardial ischemia.
      
Subsequently, the cytosolic Ca2+ concentration rises rapidly to levels that initiate contraction.
      
The effects of cyclosporine A (CsA) on Angiontensin II (Ang II)-induced protein contents, c-fos protein levels and cytosolic Ca2+ level ([Ca2+]i) in cultured cardiomyocytes of neonatal rats were observed.
      
The Ca2+ response mediated by InsP3 is not a sustained increase in the cytosolic Ca2+ concentration, but rather a series of periodic spikes that manifest as waves in larger cells.
      
Intercellular Ca2+ propagation was adenosine triphosphate-dependent and could be observed even when the target cell cytosolic Ca2+ rise was suppressed by influx of EGTA.
      
The model of membrane conductances was originally proposed for predicting membrane depolarization and voltage-dependent Ca2+ influx triggered by initial cytosolic Ca2+ increase as observed on cholinergic stimulation.
      
It is speculated that a negative insulinotropic action mediated by the calcium-sensing receptor, and possibly attributable to a fall in cytosolic Ca2+ concentration, may prevent excessive insulin secretion in pathological situations of hypercalcemia.
      
Evidence suggests that some developmentally expressed cytosolic Ca2+-binding proteins (CaBPs) have an important role in regulating or shuttling cytosolic Ca2+ since they are endowed with a high affinity for Ca2+ (~106M-1).
      
Hypotonicity also caused a rapid increase in cell volume followed by a regulatory volume decrease (RVD), cell membrane depolarization with induction of spike activity, and a rise in cytosolic Ca2+ concentration.
      
Last, the increase provoked by ouabain (1.0?mM) in cytosolic Ca2+ concentration, 45Ca fractional outflow rate and insulin release are all delayed in the ω3 rats.
      
Direct flurometric measurement of cytosolic Ca2+ under basal (unstimulated) conditions in quin 2-loaded cells revealed significantly lower concentration of free Ca2+ in carcinoma cells (≈180 nM) than in normal cells (≈200 nM).
      
 

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